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At least 19 recordsLinked to original sources
PubMed1975

Metabolic effects of exercise. II. Residual metabolic effects of exercise in rats.

This report described the duration of changes in serum lipids, adrenal weight and hepatic G-6-PD activity in rats following the termination of 10 weeks of voluntary activity in a revolving drum. Exercised rats had lower weight gain, larger adrenal glands, lower serum cholesterol, lower serum triglycerides and lower liver glucose-6-phosphate dehydrogenase (G-6-PD) activity than the sedentary controls. The differences between exercise and control rats in adrenal gland weight, body weight and G-6-PD tend to disappear within 3 wk after termination of the exercise. These experiments provide evidence that exercise can affect lipid metabolism and have a beneficial effect on the lowering of serum lipids. It also shows that this effect will persist for up to 3 wk after the exercise is terminated, under the experimental conditions of this study.

Adrenal Glands↗
PubMed1979

Vascular and metabolic effects of circulating epinephrine and norepinephrine. Concentration-effect study in dogs.

Vascular and metabolic effects of circulating epinephrine and norepinephrine have been studied in relation to the plasma concentration of these amines in dogs. Intravenous infusion of epinephrine or norepinephrine (0.1, 0.5, and 2.5 nmol x kg-1 x min-1) raised the plasma concentration of the infused amine by 2.5 , 13, and 63 nM from resting levels of 2.4 and 3.6 nM, respectively. Blood flow to isolated adipose tissue; skeletal muscle preparations; and plasma levels of glycerol, glucose, and cyclic AMP were measured. Epinephrine and norepinephrine displayed a distinct selectivity with regard to both vascular and metabolic effects. Epinephrine caused significant vasoconstriction in adipose tissue already at a plasma concentration of 5 nM, whereas no significant effect was seen on skeletal muscle vascular resistance. Norepinephrine, on the other hand, caused significant vasoconstriction in skeletal muscle at 5 nM but had no vasoconstrictor effect in adipose tissue. Epinephrine was more potent than norepinephrine in increasing plasma cyclic AMP and glucose, whereas the converse was true for plasma glycerol. Epinephrine had significant effects on plasma cyclic AMP at 5 nM and on plasma glucose and glycerol at 15 nM. Norepinephrine, on the other hand, had significant effects on plasma glycerol at 5 nM, plasma cyclic AMP at 15 nM and plasma glucose only at 65 nM. It is suggested that these response patterns are related to a preferential action of epinephrine on beta 2-adrenoceptors and a preferential action of norepinephrine on beta 1-adrenoceptors. Our results support the view that both epinephrine and norepinephrine may act as circulating hormones, because vascular and metabolic effects of both amines were seen at plasma concentrations encountered during various kinds of stress in animals and man.

Adipose Tissue↗
PubMed1978

Metabolic effects of pent-4-enoate in isolated perfused rat heart.

The metabolic effects of the hypoglycaemic agent pent-4-enoate were studied in isolated, beating or potassium-arrested rat hearts. The addition of 0.8mM-pent-4-enoate to the perfusion fluid increased O2 consumption by 76% in the arrested heart and by 14% in the beating heart; the concentration ratio of phosphocreatine/creatine increase concomitantly by 47% and 27% respectively. Perfusion of the heart with pent-4-enoate resulted in a 30-fold increase in the concentration of the pool of tricarboxylic acid-cycle intermediates in the tissue, about 90% of this increase being due to malate. The sum of the concentrations of the myocardial free amino acids remained virtually unchanged during the accumulation of the tricarboxylic acid-cycle intermediates. It was concluded that pent-4-enoate can be effectively metabolized in the myocardium and that its metabolism probably proceeds via propionyl-CoA, since pent-4-enoate reproduces many of the metabolic characteristics of propionate in the cardiac muscle. The accumulation of the tricarboxylic acid-cycle intermediates is probably due to carboxylation of propionyl-CoA. The response pattern of the metabolite concentrations in the cardiac muscle is quite different from that in the liver, in which decrease of the concentrations of the tricarboxylic acid-cycle intermediates has been observed previously [Williamson, Rostand & Peterson (1970) J. Biol. Chem. 245, 3242-3251].

Acetyl Coenzyme A↗
PubMed1975

Metabolic effects of guanethidine.

The metabolic effects of guanethidine were studied in anaesthetized rats. The drug 20 and 40 mg/kg body weight) produced a significant rise in serum free fatty acids (FFA) without significant changes in serum glucose and lactate levels. Epididymal fat pads excised from guanethidine-treated (20 mg/kg body weight) rats and incubated in vitro, exhibited an increased release of FFA and diminished uptake of glucose. Fat pads from normal rats similarly incubated in vitro in presence of various concentrations of the drug showed only a significant increase in FFA release.

Adipose Tissue↗
PubMed1978

The metabolic effects of inhaled salbutamol.

1 The metabolic effects of salbutamol (5 mg) given by intermittent positive pressure breathing have been studied in eight patients with airflow obstruction. 2 No changes in plasma nonesterified fatty acids, triglyceride, glucose, insulin or cortisol were seen 1 and 4 h after administration. 3 It is concluded that inhaled salbutamol does not cause the unwanted metabolic effects reported with oral or parenteral administration, and that this is a further indication for this route of administration.

Adult↗
PubMed1977

Metabolic effects of experimental bacteremia.

Hemodynamic and metabolic effects of a lethal 5-hour infusion of Ps. aeruginosa at a dose 10(8) organisms per ml per min were studied in 39 dogs. Blood glucose, insulin, catecholamines, body temperature, WBC, and hemodynamic parameters were measured before and at 1-hour intervals during controlled bacterial infusions. Induced bacteremia in the upper 10(4) range per ml of blood was accompanied by a decline of mean arterial blood presure from 130+/-6 mm Hg to 84+/-12 mm Hg at 4 hours, hypothermia, leukopenia, and hypoglycemia. Death within 24 hours was associated with hypoinsulinemia and increased blood catecholamines. Survival was characterized by maintenance of arterial blood pressure, only moderate decline in blood glucose levels, and normal plasma insulin concentrations with little change in plasma catecholamines. Mortality could be reduced significantly by glucose administration. This was associated with correction of hypoglycemia, rise in plasma insulin activity and increased energy production.

Animals↗
PubMed1975

Experimental study of dibutyryl cyclic AMP; its metabolic effects observed in anesthetized human subjects.

Metabolic effects of N6,O2-dibutyryl adenosine 3',5'-monophosphate (DBcAMP) were studied in 10 anesthetized patients who were divided at random into two groups each consisting of 5 patients. DBcAMP dissolved in 200 ml of physiological saline was administered intravenously at a rate of 10 mg/min for 20 min in one group and 20 mg/min for 20 min in the other group. DBcAMP infusion at either rate increased levels of blood glucose, immunoreactive plasma insulin, blood pyruvate and blood redox-potential while it reduced levels of glycerol, non-esterified fatty acid and inorganic phosphate. These findings suggest that 200 and 400 mg of DBcAMP stimulates glycogenolysis and glycolysis but inhibits lipolysis in man.

Adolescent↗
PubMed1992

The metabolic effects of oxytocin are mediated by a uterine type of receptor and are inhibited by oxytocin antagonist and by arginine vasopressin in the dog.

Infusion of oxytocin (OT) into normal dogs, in doses which produced plasma levels of OT in the physiological range, has been shown to increase plasma levels of glucose, insulin and glucagon and increase rates of glucose production and uptake. This study sought to determine whether there was a correlation between these metabolic effects and the oxytocic potency of four less potent oxytocic analogues when infused into normal dogs. The rank order of oxytocic potency of all 4 correlated well with the rise in plasma glucose levels, and in 3 of the 4 with the rise in plasma insulin levels. An antagonist of the oxytocic effect of OT suppressed the usual OT-induced rise in plasma glucose, insulin and glucagon as well as the increased glucose production and uptake. Arginine vasopressin (AVP) infusion, which by itself did not produce any metabolic effects, blocked completely the effects of OT infusion to raise plasma glucose and insulin levels and increase glucose production and uptake. The data suggest that the metabolic effects of OT in the dog are mediated by OT receptors that are similar to those producing the oxytocic effects. Whether the inhibition by AVP of the metabolic and hormonal effects of OT occurs at the receptor or post receptor level or via other mechanisms remains to be determined.

Animals↗
PubMed1975

Metabolic effects of exercise. I. Effect of exercise on serum lipids and lipogenesis in rats.

To evaluate the metabolic effects of exercise, three groups of exercised male rats were compared to their sedentary controls at the end of 10 wk of voluntary exercise in rodent activity cages. Exercises rats consumed more food than sedentary rats but had greater weight gain only at the higher levels of activity. Exercised rats had significanlty lower serum triglycerides and higher values of adipose tissue alpha-glycerophosphate dehydrogenase activity. At higher levels of physical activity, the exercised rats enhibited larger adrenal glands and lower values of hepatic glucose-6-phosphate dehydrogenase. It is concluded that specific levels of voluntary exercise are needed to achieve specific metabolic effects.

Adipose Tissue↗
PubMed1977

Mechanical and metabolic effects of diazoxide in rat uterus.

Diazoxide relaxed both polarized and depolarized rat uterus. The drug also conteracted the contractions elicited by Ca2+ in a competitive manner. The relaxing effect was associated with an increase in the tissue level of cyclic AMP. This metabolic effect of diazoxide was inhibited by propranolol-treatment and in preparations from reserpinized animals, while the mechanical effects were only partially reduced. Diazoxide was also found to increase the release of tritium from preparations preloaded with [3H]-noradrenaline. It is suggested that diazoxide may induce some of its mechanical and metabolic effects by releasing the adrenergic transmittor substance noradrenaline. An effect of diazoxide on the Ca2+-metabolism is also probable.

Animals↗
PubMedDate not supplied

Metabolic effects of glucagon in endogenous hypertriglyceridemia.

The metabolic effects of glucagon, administered i.v. in doses of 1 microgram/kg, were evaluated in two groups of patients with endogenous hypertriglyceridemia (Types IV and V according to Fredrickson) with normal and reduced glucose tolerance and in a control group. Glucagon had a lipolytic effect, evaluated as the plasma increase of free fatty acids (FFA) during the first 20 min in normal subjects, but not in the two hyperlipemic groups. A negative correlation was observed between fasting IRI level and FFA mobilization. The ketogenic and hypotriglyceridemic effects of glucagon were demonstrated in normal and hyperlipemic groups. It would seem, therefore, that at the pharmacological doses injected, there is no resistance to the hypotriglyceridemic effect of glucagon in endogenous hypertriglyceridemia.

Adult↗
PubMed1992

Metabolic effects of proglycosyn.

Proglycosyn, a phenylacyl imidazolium compound that lowers blood glucose levels, was demonstrated previously to promote hepatic glycogen synthesis, stabilize hepatic glycogen stores, activate glycogen synthase, inactivate glycogen phosphorylase, and inhibit glycolysis. In the present study proglycosyn was found to inhibit fatty acid synthesis, stimulate fatty acid oxidation, and lower fructose 2,6-bisphosphate levels, but to have no significant effects on cell swelling and the levels of cAMP in hepatocytes prepared from fed rats. Verapamil and atropine blocked the effects of proglycosyn on glycogen metabolism, but these compounds inhibit proglycosyn accumulation by hepatocytes. Proglycosyn stimulated phosphoprotein phosphatase activity in postmitochondrial extracts, as measured by dephosphorylation of phosphorylase a and glycogen synthase D, but this action required a very high concentration of the compound, making it unlikely to be the actual mechanism involved. It is proposed that a metabolite of proglycosyn is responsible for its metabolic effects.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

Bilateral cerebral metabolic effects of pharmacological manipulation of the substantia nigra in the rat: unilateral intranigral application of the putative excitatory neurotransmitter substance P.

The metabolic activity of several anatomically distinct brain areas was investigated by means of the quantitative autoradiographic 2-deoxy-D[1-14C]glucose method in awake rats following unilateral intranigral application of the putative excitatory neurotransmitter substance P. The primary goal was to determine the metabolic effects of substance P on the substantia nigra and its targets. Intranigral injection of 1 mM substance P (1.5 microliters) induced metabolic activation locally in the substantia nigra reticulata by 117% and substantia nigra compacta by 35%, as well as distally in the contralateral substantia nigra reticulata by 22% and contralateral substantia nigra compacta by 21%. All the basal ganglia components, the striatum, pallidum, entopeduncular, subthalamic nucleus and nucleus accumbens displayed bilateral metabolic activations after unilateral intranigral substance P injection. Among the principal reticulata efferent projections, the ventromedial, ventrolateral, parafascicular, mediodorsal and centrolateral thalamic nuclei, as well as the pedunculopontine nucleus displayed bilateral metabolic activations after intranigral substance P application. Moreover, unilateral intranigral substance P injection elicited metabolic activations in the thalamic and cortical components of the reticular, intralaminar, limbic and prefrontal systems, mostly bilateral. It is suggested that substance P applied into one substantia nigra reticulata activates the compacta nigrostriatal dopaminergic and the reticulata nigrothalamic GABAergic outputs inducing distal metabolic effects, similar to those elicited by unilateral nigral electrical stimulation [Savaki et al. (1983) J. comp. Neurol. 213, 46-65] and, opposite to several of those induced by intranigral injection of the inhibitory GABAA agonist muscimol [Savaki et al. (1992) Neuroscience 50, 781-794]. Furthermore, it is suggested that the ipsilateral basal ganglia effects induced by intranigral substance P application are mediated via both the compacta dopaminergic nigrostriatal projection and the reticulata GABAergic nigro-thalamocortico-striatal loop, whereas the contralateral basal ganglia and associated thalamocortical effects are due to the activation of the GABAergic reticulata efferents and are mediated via an interthalamic circuitry involving the motor, reticular and intralaminar thalamic nuclei.

Animals↗
PubMed1977

Cytologic and metabolic effects of prostaglandins on rat skin.

The cellular and metabolic effects of exogenous prostaglandins E1, E2, and F2alpha (PGE1, PGE2, and PGF2alpha) were studied in the skin of rats by using scintillation counting, autoradiography, electron microscopy, and scanning electron microscopy. Radioactivity measurements demonstrated that prostaglandins of the E series induced a marked increase in the incorporation of [3H]leucine, [3H]thymidine, [3H]uridine, and [3H]proline in the rat skin, mostly at 1 hr, whereas PGF2alpha inhibited this phenomenon. Light microscopic autoradiography revealed an increased incorporation of [3H]leucine in the cytoplasm of hyperplastic epidermis of PGE-treated rats; also, the incorporation of [3H]thymidine, [3H]uridine, and [3H]proline was significantly increased over the epidermal nuclei, nucleoli, and the collagen fibers of PGE-treated rats. Electron microscopy revealed ultrastructural changes of the epidermal cells and fibroblasts following PGE administration, including an increase in polyribosomes, endoplasmic reticulum, keratohyaline granules, and enlarged intercellular spaces; PGF2alpha induced advanced cytolysis and cell disintegration, with increased lysosome formation. Scanning electron microscopy showed hypertrophied collagen fibers in PGE-treated rats; however, a disruption and disintegration of collagen fibers occurred in PGF2alpha-treated rats. The level of PGE1 in the skin of treated rats was markedly elevated as compared to those of controls. These findings demonstrate that prostaglandins are potent regulators for the epidermal cell ultrastructure and metabolism as well as for collagen synthesis.

Animals↗
PubMed1979

Metabolic effects of blood flow restriction in adipose tissue.

The metabolic effects of blood flow restriction were studied in isolated blood-perfused canine subcutaneous adipose tissue. Blood flow restriction (on the average to 20 per cent of control flow) was caused by either mechanical clamping of the arterial inflow or by i.a. injections of methoxamine or angiotensin. Glucose uptake in the adipose tissue was reduced during blood flow restriction. This was partially compensated for by a period of increased glucose uptake following restoration of flow. Blood flow restriction also caused an increase in the venous lactate/pyruvate ratio. The basal lipolytic rate was decreased during blood flow restriction. Lipolysis induced by brief (5 min) sympathetic nerve stimulation (4 Hz) was not inhibited by blood flow restriction as the total amount of glycerol released from the tissue was unaffected. The outflow rate was reduced during blood flow restriction, but glycerol trapped within the tissue was apparently not reutilized by the fat cells as it was released upon flow restroation. FFA outflow following nerve stimulation was, however, inhibited suggesting increased reutilization of FFA within the tissue. This increased reutilization may ultimately be caused by the observed change in red./ox.-balance and/or by the limited carrier capacity (albumin) available during blood flow restriction. Three main conclusions may be drawn from the present results. Firstly, plasma levels of glycerol and FFA do not necessarily reflect adipose tissue lipolysis at a given moment. Secondly, the decreased adipose tissue blood flow seems to be a major cause of the lowered FFA-levels during hemorrhage. Thirdly, in contrast to hemorrhage, even severe reduction of adipose tissue blood flow is insufficient to cause irreversible ischemic damage.

Adipose Tissue↗
PubMed1977

Metabolic effects of sodium restriction and thiazides in tetraplegic patients.

The metabolic effects of sodium restriction, alone or with thiazide, were studied in 12 healthy subjects, in 24 tetraplegics during the intial 8 months of paralysis (early) and in 16 others during the subsequent period (late). The diuresis caused by both treatments led to more haemoconcentration in early than in late patients. In contrast with the healthy subjects on low sodium, the tetraplegics had a delayed urinary sodium retention and no fall in calciuria. During thiazide, urinary sodium depletion occurred early and the urine calcium fell after 3 days in all tetraplegics. During both treatments, aldosterone and renin increased more in early patients than in the other groups. The clinical implications of inducing dehydration and a sustained stimulation of the renin-angiotensin-aldosterone axis in recently injured tetraplegics with severe orthostatic hypotension are discussed.

Adolescent↗
PubMed1978

Circulatory and metabolic effects in the brain induced by amphetamine sulphate.

Cerebral circulatory and metabolic effects of amphetamine sulphate (0.25-25 mg.kg-1 i.v. or 5-10 mg.kg-1 i.p.) were studied in anesthetized, paralyzed and artifically ventilated rats. Cerebral blood flow (CBF) was measured with a modification of the Kety and Schmidt (1948) technique, and oxygen consumption (CMRO2) was calculated from CBF and arteriovenous differences in oxygen content. Regional CBF was evaluated from the uptake of 14C-ethanol. Cortical metabolites were analysed following freezing of tissue in situ. Amphetamine administration gave rise to a marked increase in CBF that was doubled following 0.25 mg.kg-1 and increased 4-fold following 15 mg.kg-1. However, such excessive increases in flow were confined to frontoparietal cortical regions, while other cortical or subcortical areas showed more moderate hyperemia. The increase in CBF was unrelated to changes in arterial PCO2, blood pressure, or tissue lactate content. CMRO2 increased by 30% to 95% depending on dose and rat strain used. At all doses employed, amphetamine gave rise to glycogenolysis in cerebral cortex but, in animals studied within the first 30 min after 5 mg.kg-1, or less, the only other changes were increases in glucose-6-phosphate and alpha-ketoglutarate concentrations. When the dose was increased to 15 mg.kg-1, there were moderate increased in lactate concentration and lactate/pyruvate ratio. Sixty min after 5 mg.kg-1 there were increases in tissue concentrations of pyruvate, citric acid cycle intermediates and alanine, as well.

Amphetamine↗
PubMed1977

Relative toxicity and metabolic effects of cholecalciferol and 25-hydroxycholecalciferol in chicks.

The relative toxicity and metabolic effectiveness of cholecalciferol (CC) and 25-hydroxycholecalciferol (25-HCC) in chicks were evaluated by feeding six graded levels of each and observing gross and microscopic pathology as well as several metabolic parameters of calcium metabolism. Renal tubular calcification was observed when CC was fed at the rate of 10.0 mg/kg of diet and when 25-HCC was fed at the rate of 0.1 mg/kg diet. Thus, 100-fold increase in toxicity results when the hydroxylated form of CC is fed. Both microscopic renal lesions and increased renal calcium and inorganic phosphate concentrations occurred in chicks with normal serum calcium concentrations.

Alkaline Phosphatase↗